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be phosphorylated and activated by AtCPK21 and AtCPK23 in response to ABA
(Geiger et al. 2010 , 2011 ; Demir et al. 2013 ). However, AtCPK6 and AtCPK23
preferentially phosphorylate and activate SLAC1 and SLAH3 independently of
Ca 2 + , whereas AtCPK3 and AtCPK21 mainly regulate these channels in a Ca 2 + -
dependent manner (Brandt et al. 2012 ; Scherzer et al. 2012 ). This suggests that
AtCPK6 and AtCPK23, together with the OST1 kinase (see next section), may be
associated with Ca 2 + -independent signaling steps, whereas AtCPK3 and AtCPK21
may regulate Ca 2 + -dependent SLAC1 and SLAH3 activation in ABA signal-
ing in guard cells. It remains to explore the underlying mechanism how these
CDPKs function distinctly in relation to Ca 2 + dependence in the ABA-mediated
anion channel activation to understand stomatal regulation in response to ABA.
Importantly, a signaling pathway has been described from ABA signal percep-
tion to the CDPK-mediated activation of the SLAC1 and SLAH3 anion channels,
where the PYR/PYL/RCAR family ABA receptor members PYR1 and RCAR1
inhibit a type 2C protein phosphatase member ABI1 to release AtCPK3/6/21/23
from inhibition, leading to Ca 2 + -dependent activation of the anion channels
of guard cells in response to ABA (Geiger et al. 2010 , 2011 ; Brandt et al. 2012 ;
Scherzer et al. 2012 ; Demir et al. 2013 ). See Fig. 8.2 and Chap. 6 of this topic).
Fig. 8.2 A summary of the protein kinases and phosphatases involved in ABA signaling and
their possible functional mechanisms in the model plant Arabidopsis . See detailed description in
the text. Arrows denote positive regulation or activation, and bars denote negative regulation or
repression. The solid lines indicate direct effect and dotted lines indirect effect. Question mark
indicates unconfirmed link
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